HEPATIC VENOOCCLUSIVE DISEASE AFTER BONE-MARROW TRANSPLANTATION - IMMUNOHISTOCHEMICAL IDENTIFICATION OF THE MATERIAL WITHIN OCCLUDED CENTRAL VENULES

  • 1 June 1987
    • journal article
    • research article
    • Vol. 127  (3) , 549-558
Abstract
The authors immunostained autopsy liver tissue from 31 marrow transplant recipients, 19 with hepatic venoocclusive disease (VOD) and 12 without VOD. A panel of monoclonal and polyclonal antibodies was used to characterize the materials within the occluded venous lesions and to define the location and types of injured cells. Most patients with early VOD (survival < 50 days, n = 11) had dense periadventitial and intramural immunostaining of terminal hepatic and sublobular central venules (CV) with anti-Factor VIII (9/11) and anti-fibrinogen (4/4) but had no immunostaining with antibody to platelet GPIb. Early VOD patients also had marked loss of Zone 3 hepatocyte cytokeratin (8/9) versus late VOD (1/5) or non-VOD (2/7). Patients with late VOD lesions (n = 8, survival > 50 days) had increased collagens within occluded VOD lesions, Type III > > Type I, and increased sinusoidal collagens Types I, III, and IV. These studies and other data suggest the following events in the genesis of VOD. Initial injury to endothelium of CV and/or sinusoids and possibly also to Zone 3 hepatocytes triggers the coagulation cascade in the periadventitial zone of CV. The late sequela, collagenous CV occlusion, results from activated mural myofibroblasts and/or embolized Ito cells and hepatocytes.